ArticleProceedings of the National Academy of Sciences of the United States of America2020
IL-4 controls activated neutrophil FcγR2b expression and migration into inflamed joints.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 42 citations in OpenAlex.
- A multiplex, prime editing framework for identifying drug resistance variants at scale.Cell genomics · 2026Article
- CD44v5 enhances the IL-4/IL-4Rα/STAT6/SAM68 aix inducing M2 polarization and promoting triple-negative breast cancer progression.Cancer biology & therapy · 2025Article
- Interleukin-4 and clinical activity in rheumatoid arthritis: a sex-based analysis.Advances in rheumatology (London, England) · 2025Article
- Comprehensive Profiling of Cytokines and Growth Factors: Pathogenic Roles and Clinical Applications in Autoimmune Diseases.International journal of molecular sciences · 2025Review
- Pathogenic Role of Cytokines in Rheumatoid Arthritis.Journal of clinical medicine · 2025Review
- Advances in the application and research of biomaterials in promoting bone repair and regeneration through immune modulation.Materials today. Bio · 2025Review
- Proteomic analysis of exosomes fromFrontiers in immunology · 2025Article
- Cytokine polarized, alternatively activated bone marrow neutrophils drive axon regeneration.Nature immunology · 2024Article
- Human and mouse neutrophils share core transcriptional programs in both homeostatic and inflamed contexts.Nature communications · 2023Article
- Article
- Eosinophil-derived IL-4 is necessary to establish the inflammatory structure in innate inflammation.EMBO molecular medicine · 2023Article
- Interleukin-4 during post-exercise recovery negatively correlates with the production of phagocyte-generated oxidants.Frontiers in physiology · 2023Article
- Arrayed CRISPR/Cas9 Screening for the Functional Validation of Cancer Genetic Dependencies.Bio-protocol · 2022Article
- Patients with systemic sclerosis show phenotypic and functional defects in neutrophils.Allergy · 2022Article
- The Interactions Between Autoinflammation and Type 2 Immunity: From Mechanistic Studies to Epidemiologic Associations.Frontiers in immunology · 2022Review
- Alzheimer's disease-associated inflammatory pathways might contribute to osteoporosis through the interaction betweenFrontiers in neurology · 2022Article
- CRISPR/Cas9-Induced DNA Damage Enriches for Mutations in a p53-Linked Interactome: Implications for CRISPR-Based Therapies.Cancer research · 2022Article
- Review
- A rapid CRISPR competitive assay forComputational and structural biotechnology journal · 2021Article
- Curcumin Mitigates AFB1-Induced Hepatic Toxicity by Triggering Cattle Antioxidant and Anti-inflammatory Pathways: A Whole Transcriptomic In Vitro Study.Antioxidants (Basel, Switzerland) · 2020Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neutrophils are the most abundant immune cells found in actively inflamed joints of patients with rheumatoid arthritis (RA), and most animal models for RA depend on neutrophils for the induction of joint inflammation. Exogenous IL-4 and IL-13 protect mice from antibody-mediated joint inflammation, although the mechanism is not understood. Neutrophils display a very strong basal expression of STAT6, which is responsible for signaling following exposure to IL-4 and IL-13. Still, the role of IL-4 and IL-13 in neutrophil biology has not been well studied. This can be explained by the low neutrophil surface expression of the IL-4 receptor α-chain (IL-4Rα), essential for IL-4- and IL-13-induced STAT6 signaling. Here we identify that colony stimulating factor 3 (CSF3), released during acute inflammation, mediates potent STAT3-dependent neutrophil IL-4Rα up-regulation during sterile inflammatory conditions. We further demonstrate that IL-4 limits neutrophil migration to inflamed joints, and that CSF3 combined with IL-4 or IL-13 results in a prominent neutrophil up-regulation of the inhibitory Fcγ receptor (FcγR2b). Taking these data together, we demonstrate that the IL-4 and CSF3 pathways are linked and play important roles in regulating proinflammatory neutrophil behavior.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.